The use of transverse thermoelectric effects in magnetic materials is expected to simplify the structure of thermoelectric conversion devices compared to the longitudinal thermoelectric effects, where electric and thermal currents are converted in parallel directions. This simplification can lead to enhanced versatility and durability of the devices, as well as cost reduction. The main focus of the development of magnetic materials for transverse thermoelectric conversion has been the exploration of new alloys based on electronic structure, with no research on the microstructure within the materials.

The team has now demonstrated that a simple three-minutes heat treatment of an iron-based amorphous alloy, without changing the average composition of the material, significantly improves the performance of the anomalous Nernst effect — one of the transverse thermoelectric effects. The anomalous Nernst coefficient, obtained at the optimal heat treatment temperature, showed the highest value known among magnetic amorphous alloys, and the improvement was found to be significantly influenced by nano-sized copper precipitates within the alloy. This result suggests that not only the electronic structure and composition of the material but also the design and control of the microstructure are important for enhancing the anomalous Nernst coefficient.

The developed magnetic material can be easily mass-produced and scaled up, and it is also flexible. By further developing magnetic materials with even higher anomalous Nernst coefficients through microstructure control, the team aims to apply this technology to energy conversions in electronic devices and to thermal sensing technologies.

Publishing in the journal Cell Host & Microbe, the study describes an approach that provides step-by-step directions for the immune system to generate the elusive, yet necessary antibodies for a successful HIV vaccine.

“HIV is the fastest-evolving virus known. So it’s been a long-standing goal in HIV research to create a vaccine that can generate broadly neutralizing antibodies that can recognize diverse HIV strains,” said lead author Kevin Wiehe, Ph.D., associate professor in the Department of Medicine at Duke University School of Medicine and director of research at DHVI.

Wiehe and colleagues started with an engineered version of a broadly neutralizing antibody in its original state, before any mutations occurred. Knowing that the antibody will need to mutate to keep up with the ever-changing HIV virus, the researchers then added sequential mutations one-by-one to determine which mutations were essential for the antibody to broadly neutralize HIV.

Doing this allowed them to figure out what the exact points were along the route to arrive at broadly neutralizing antibodies. They then developed a vaccine which gave the immune system the turn-by-turn directions to follow that mutational route.

Using mice specially bred to encode for the original version of the antibody, the researchers demonstrated that the guidance system approach triggered the immune system to start churning out the sought-after antibodies.

“This paper shows that our mutation-guided vaccine strategy can work,” said Wiehe, adding that the technique could also be used in vaccines for other diseases. “This strategy potentially gives us a way to design vaccines to direct the immune system to make any antibody we want, which could be a broadly neutralizing antibody for all coronavirus variants, or an anti-cancer antibody.”

Wiehe said the next challenge will be to reproduce the study in primates and then humans.

In addition to Wiehe, study authors includes Kevin O. Saunders, Victoria Stalls, Derek W. Cain, Sravani Venkatayogi, Joshua S. Martin Beem, Madison Berry, Tyler Evangelous, Rory Henderson, Bhavna Hora, Shi-Mao Xia, Chuancang Jiang, Amanda Newman, Cindy Bowman, Xiaozhi Lu, Mary E. Bryan, Joena Bal, Aja Sanzone, Haiyan Chen, Amanda Eaton, Mark A. Tomai, Christopher B. Fox, Ying Tam, Christopher Barbosa, Mattia Bonsignori, Hiromi Muramatsu, S. Manir Alam, David Montefiori, Wilton B. Williams, Norbert Pardi, Ming Tian, Drew Weissman, Frederick W. Alt, Priyamvada Acharya, and Barton F. Haynes.

The study received funding support from the National Institute of Allergy and Infectious Diseases, a part of the National Institutes of Health (UM1AI144371, 1U19AI135902-01, P01AI131251-01).

The research links interpersonal discrimination to changes at the molecular level, revealing a potential root cause of disparities in aging-related illness and death.

“Experiencing discrimination appears to hasten the process of aging, which may be contributing to disease and early mortality and fueling health disparities,” said Adolfo Cuevas, assistant professor in the Department of Social and Behavioral Sciences at NYU’s School of Global Public Health and senior author of the study published in the journal Brain, Behavior, and Immunity-Health.

Research shows that people who experience discrimination based on their identity (e.g. race, gender, weight, or disability) are at increased risk for a range of health issues, including heart disease, high blood pressure, and depression. While the precise biological factors driving these poor health outcomes are not fully understood, chronic activation of the body’s stress response is a likely contributor. Moreover, a growing body of research connects persistent exposure to discrimination to the biological processes of aging.

To better understand the connection between discrimination and aging, Cuevas and his colleagues looked at three measures of DNA methylation, a marker that can be used to assess the biological impacts of stress and the aging process. Blood samples and surveys were collected from nearly 2,000 U.S. adults as part of the Midlife in the United States (MIDUS) study, a longitudinal analysis of health and well-being funded by the National Institute on Aging.

Participants were asked about their experiences with three forms of discrimination: everyday, major, and workplace. Everyday discrimination refers to subtle and minor instances of disrespect in daily life, whereas major discrimination focuses on acute and intense instances of discrimination (for example, being physically threatened by police officers). Discrimination in the workplace includes unjust practices, stunted professional opportunities, and punishment based on identity.

The researchers found that discrimination was linked to accelerated biological aging, with people who reported more discrimination aging faster biologically compared to those who experienced less discrimination. Everyday and major discrimination were consistently associated with biological aging, while exposure to discrimination in the workplace was also linked to accelerated aging, but its impact was comparatively less severe.

A deeper analysis showed that two health factors — smoking and body mass index — explained roughly half of the association between discrimination and aging, suggesting that other stress responses to discrimination, such as increased cortisol and poor sleep, are contributing to accelerated aging.

“While health behaviors partly explain these disparities, it’s likely that a range of processes are at play connecting psychosocial stressors to biological aging,” said Cuevas, who is also a core faculty at the Center for Anti-racism, Social Justice, & Public Health at NYU School of Global Public Health.

In addition, the link between discrimination and accelerated biological aging varied by race. Black study participants reported more discrimination and tended to exhibit older biological age and faster biological aging. However, White participants, who reported less discrimination, were more susceptible to the impacts of discrimination when they did experience it, perhaps due to less frequent exposure and fewer coping strategies. (Data on other racial and ethnic groups were not available in the MIDUS study.)

“These findings underscore the importance of addressing all forms of discrimination to support healthy aging and promote health equity,” added Cuevas.

In addition to Cuevas, study authors include Steven W. Cole of the University of California, Los Angeles; Daniel W. Belsky of Columbia University; and Anna-Michelle McSorley, Jasmine M. Shon, and Virginia W. Chang of the NYU School of Global Public Health.

The MIDUS study is supported by the John D. and Catherine T. MacArthur Foundation Research Network and the National Institute on Aging (P01-AG020166 and U19-AG051426). The study itself was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (R01DK137246 and R01DK137805).